Investigation of methicillin-resistant Staphylococcus aureus showing reduced vancomycin susceptibility isolated from a patient with infective endocarditis

Takayama, Yoko; Hanaki, Hideaki; Irinoda, Kazuhiko; Kokubun, Hideya; Yoshida, Kazunari; Sunakawa, Keisuke

doi:10.1016/s0924-8579(03)00263-2

Cited by 9 publications

(10 citation statements)

References 22 publications

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“…As described above, in many cases, the hVISA or VISA phenotype is detected after a prolonged period of infection, which is associated with a failure of glycopeptide therapy (121,151,213,313,316,326,337,340,348,376). The testing of later clinical isolates from patients who have failed glycopeptide treatment appears more likely to yield a positive result for hVISA or VISA.…”

Section: Practical Approach To Hvisa and Visa Detectionmentioning

confidence: 98%

“…For many patients, the hVISA or VISA phenotype was detected in bacterial isolates only after a prolonged period of infection associated with the failure of glycopeptide therapy (48,121,124,151,213,313,316,326,337,340,376). In many of these cases, a detailed analysis of the earlier clinical isolate failed to detect any vancomycin heteroresistance, and the phenotype appears to have emerged from a vancomycin-susceptible strain during therapy.…”

Section: Global Epidemiology and Associated Features Of Hvisa And Visamentioning

confidence: 99%

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Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

et al. 2010

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SUMMARY The emergence of vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA) over the past decade has provided a challenge to diagnostic microbiologists to detect these strains, clinicians treating patients with infections due to these strains, and researchers attempting to understand the resistance mechanisms. Recent data show that these strains have been detected globally and in many cases are associated with glycopeptide treatment failure; however, more rigorous clinical studies are required to clearly define the contribution of hVISA to glycopeptide treatment outcomes. It is now becoming clear that sequential point mutations in key global regulatory genes contribute to the hVISA and VISA phenotypes, which are associated predominately with cell wall thickening and restricted vancomycin access to its site of activity in the division septum; however, the phenotypic features of these strains can vary because the mutations leading to resistance can vary. Interestingly, changes in the staphylococcal surface and expression of agr are likely to impact host-pathogen interactions in hVISA and VISA infections. Given the subtleties of vancomycin susceptibility testing against S. aureus, it is imperative that diagnostic laboratories use well-standardized methods and have a framework for detecting reduced vancomycin susceptibility in S. aureus.

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Section: Practical Approach To Hvisa and Visa Detectionmentioning

confidence: 98%

Section: Global Epidemiology and Associated Features Of Hvisa And Visamentioning

confidence: 99%

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

et al. 2010

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“…Antibiotics available for the treatment of such patients may be a combination of VAN and ␤-lactam antibiotics. We reported recently that VAN-resistant MRSA emerged as a result of the simultaneous use of VAN and ␤-lactam antibiotics (15,26). A hospital outbreak of BIVR infection was reported previously (16).…”

Section: Discussionmentioning

confidence: 99%

“…In fact, a synergistic effect of these drugs was previously reported (9,22). However, the combination therapy of VAN and a ␤-lactam antibiotic caused the emergence of VAN-resistant MRSA (15,26), designated ␤-lactaminduced VAN-resistant MRSA (BIVR) (12,14). Currently, about 20% of MRSA strains isolated from septicemia patients have been reported to be BIVR (13).…”

mentioning

confidence: 99%

Rapid Depletion of Free Vancomycin in Medium in the Presence of β-Lactam Antibiotics and Growth Restoration in Staphylococcus aureus Strains with β-Lactam-Induced Vancomycin Resistance

Yanagisawa

Hanaki

Matsui

et al. 2009

Antimicrob Agents Chemother

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Growth of the BIVR cells to an absorption level of ϳ0.3 at 578 nm required about 24 h in the presence of vancomycin alone at the MIC (4.0 g/ml). However, growth was achieved in only about 10 h when 1/1,000 to 1/2,000 the MIC of ␤-lactam antibiotic was added 2 h prior to the addition of vancomycin, suggesting that the ␤-lactams shortened the time to recovery from vancomycin-mediated growth inhibition. Free vancomycin in the culture medium decreased to 2.3 g/ml in the first 8 h in the culture containing vancomycin alone, yet cell growth was undetectable. When the vancomycin concentration dropped below ϳ1.5 g/ml at 24 h, the cells began to grow. In the culture supplemented with the ␤-lactam 2 h prior to the addition of vancomycin, the drug concentration continuously dropped from 4 to 0.5 g/ml in the first 8 h, and the cells began to grow at a vancomycin concentration of ϳ1.7 g/ml or at 4 h of incubation. The gene encoding the enzyme involved in D-Ala-D-lactate synthesis was undetectable. Based on these results, we concluded that BIVR is attributable mainly to a rapid depletion of vancomycin in the medium triggered or promoted by ␤-lactam antibiotics.

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“…Infections caused by heteroresistant VISA are associated with a protracted clinical course, as has been shown in a study of hVISA bacteremia, which persisted for 7 days more in a larger proportion of patients than did MRSA bacteremia [79]. Therefore, reduced susceptibility to vancomycin should be suspected in patients with MRSA infection that does not improve despite adequate vancomycin levels [80]. In a study of 22 patients with persistent or recurrent MRSA bacteremia, heteroresistance to vancomycin was found in three (13.6%) isolates, suggesting that heteroresistance may be a relevant cause of treatment failure [81].…”

Section: Clinical Impact Of Glycopeptide Resistancementioning

confidence: 91%

Epidemiology and Clinical Impact of Glycopeptide Resistance in Staphylococcus aureus

Ruef

2004

Infection

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Investigation of methicillin-resistant Staphylococcus aureus showing reduced vancomycin susceptibility isolated from a patient with infective endocarditis

Cited by 9 publications

References 22 publications

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

Rapid Depletion of Free Vancomycin in Medium in the Presence of β-Lactam Antibiotics and Growth Restoration in Staphylococcus aureus Strains with β-Lactam-Induced Vancomycin Resistance

Epidemiology and Clinical Impact of Glycopeptide Resistance in Staphylococcus aureus

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